HIV/AIDS Skepticism

Pointing to evidence that HIV is not the necessary and sufficient cause of AIDS

Posts Tagged ‘HIV in pregnancy’

Spontaneous generation of “HIV”

Posted by Henry Bauer on 2009/10/25

In places where claimed outbreaks of “HIV” have had “infected needles” as the only possible source of the supposedly infecting agent, the large but unaddressed question is, how did those needles become infected in the first place? And then remain infected long enough to pass on that infection when the purported contagious agent is supposed to survive for only a brief time outside bodily fluids? [HIV/AIDS in Italy — and “NEEDLE ZERO”, 11 October 2008; “Needle ZERO” again; or, HIV pops up magically out of nowhere, 15 November 2008].
It’s as though this “HIV” were spontaneously generating itself. That would not have seemed absurd a couple of centuries ago, when spontaneous generation of living organisms was an acceptable theory, but HIV/AIDS theory is supposed to be scientifically up-to-date.

An even more direct instance of “HIV-positive” in absence of “HIV” is that of certain elite controllers who have no detectable “viral load” (Compounding HIV/AIDS absurdities, 11 October 2009).

There are at least two other situations where “HIV-positive” pops up without any sign that “HIV” was present in the first place: In clinical trials of circumcision as a means of preventing “HIV-positive” status, and in a prospective study of acquisition of “HIV” by pregnant women.


Two clinical trials of circumcision both reported that participants in both control and intervention groups acquired “HIV-positive” status during the trial even while abstaining from intercourse:

“there were seven early seroconverters . . . : four in the circumcision group and three in the control group. Three of the four in the circumcision group reported no sexual activity in the month after circumcision. We cannot exclude the possibility that any of these individuals were actually HIV positive at baseline, and that their infection was not detected. Two of the three early seroconverters in the control group also denied sexual activity in the period before seroconversion” [emphases added; Bailey et al., “Male circumcision for HIV prevention in young men in Kisumu, Kenya: a randomised controlled trial”, Lancet, 369 (2007) 643-56].

circumcision  was not protective against HIV acquisition in the few men  who  reported  no  sexual  activity in  a  given  follow-up  interval. There were six incident cases (three in each group)  during periods of reported abstinence. None of these six  participants reported receipt of injections or transfusions  during the follow-up interval of HIV seroconversion; these  participants probably under-reported their sexual activity” [emphases added; Gray et al., “Male circumcision for HIV prevention in men in Rakai, Uganda: a randomised trial”, Lancet, 369 (2007) 657-66].

The mainstream explanation, then, is that the individuals concerned lied, or that they had been “HIV-positive” at enrolment but failed to be detected by those highly specific “HIV” tests. Sherlock Homes might have agreed in general that when all the likely possibilities have been excluded, one must accept those of high improbability — but Holmes would never have come to believe HIV/AIDS theory in the first place. What a coincidence, that about the same number of men in all four groups became “HIV-positive” in absence of sexual activity. Or, alternatively, what a coincidence that the number who not only lied about sexual activity but also became “HIV-positive” should be the same in all four groups.

HIV Skeptics and AIDS Rethinkers, however, understand that “HIV-positive” does not necessarily bespeak an infection transmitted sexually or by other means. These facts are perfectly compatible with the copious data that show “HIV-positive” to be a condition inducible by any number of stimulating influences. Moreover, the tendency to test “HIV-positive” increases with age from the teens into middle age:


Therefore it is only to be expected that in any group of young men observed for any substantial length of time, a few will become “HIV-positive” — perhaps as a result of flu, or malaria, or a vaccination, etc.


Consistent with these occasional real-time observations of “HIV-positive” incidence among people who have had no sexual activity, no blood transfusions, and no injections is the finding in a large clinical trial carried out over many years that pregnant women become “HIV-positive” at a greater rate than do those who have already given birth and are lactating or those who are neither pregnant nor breastfeeding:


Lest one attempt to explain this away by postulating, counter to common sense, that pregnant women have more sex or more unsafe sex than do non-pregnant women, Gray et al. note that
“The  mean  monthly  frequency  of  intercourse  was  lower  during  pregnancy  (6·7  acts  per month) than during breastfeeding (7·5 acts per month) and  during  non-pregnant  and  non-lactating  intervals (8·0 per month; p<0·05). Therefore, we also estimated the  rate  of  HIV  acquisition  per  coital  act,  which  was higher during pregnancy than in the non-pregnant and non-lactating group (incidence rate ratio 1·42, 95% CI 0·37-3·82). . . . [P]regnant women were  significantly  less  likely  to  report  multiple  sexual partners  than  were  non-pregnant  and  non-lactating women,  and   in   married   couples   the   husbands   of pregnant  women  reported  significantly  fewer  sexual partners  than  husbands  of  non-pregnant  and  non- lactating women. Although there could be misreporting of  sexual  behaviours,  the  results  are  unlikely  to  differ between the three exposure groups, so both female and male  sexual  behaviours  are  unlikely  to  account  for  the excess risk of HIV during pregnancy. . . . [W]e  conclude  that  behavioural  factors  are unlikely  to  explain  why  the  HIV  incidence  rate  is increased  during  pregnancy,  and  we  speculate  that biological factors might have a role. . . . . Hormonal  contraception  has  been  associated  with  increased  risks  of  HIV acquisition   in   some   but   not   all   epidemiological studies” [emphases added].
In overall summary, Gray et al. state:
“Interpretation The risk of HIV acquisition rises during pregnancy. This change is unlikely to be due to sexual risk behaviours, but might be attributable to hormonal changes affecting the genital tract mucosa or immune responses. HIV prevention efforts are needed during pregnancy to protect mothers and their infants.”

How close they come to recognizing the fact of the matter, that “HIV-positive” signifies any one or more of a wide range of physiological conditions, of which pregnancy has long been known to be one. They even cite a study from Malawi that reported higher incidence of “HIV-positive” in pregnancy than post-partum, by a factor of 2.19, and another from Rwanda that reported higher incidence of “HIV-positive” early post-partum compared to later. In South Africa, “HIV-positive” prevalence is persistently higher among pregnant women than among women as a whole [HIV demographics are predictable; HIV is not a contagious infection, 27 August 2008].


But perhaps most remarkable of all is the quite direct evidence in the Gray article that “HIV” can be “caught” in absence of “HIV”. During the study, 338 seroconversions were observed: 23 among pregnant women, 40 among lactating women, and 275 among the others. The article also reports on discordant couples — male partner “HIV-positive”, wife “HIV”-negative — and in those cases there were 77 seroconversions: 6 among pregnant women, 11 among lactating women, and 60 among the rest. The inference is clear that 261 (338-77) seroconversions occurred among couples not known to be discordant — in other words, one partner “caught” “HIV” though the other partner didn’t have it.

Of course, “partners not known to be ‘HIV-positive’” is not the same as “partners known not to be ‘HIV-positive’”. But since the investigators explicitly sought to ascertain the “HIV” status of partners, and were confident enough of their data that they reported separately on “transmission” among discordant couples, it seems unlikely that they would have missed a large enough number to explain all the seroconversions observed in the study; therefore it does seem that as many as 77% (261/338) of the women in the study who became “HIV-positive” did so without any evidence of sexual intercourse with an “HIV-positive” male, indeed, with implicit evidence of LACK of such contact.

Lest this line of inference not be convincing, consider this clear statement in the article’s Summary:
“In married pregnant women who had a sexual relationship with their male spouses, the HIV incidence rate ratio was 1·36  (0·63-2·93).  In  married  pregnant  women  in  HIV-discordant  relationships  (ie,  with  HIV-positive  men)  the incidence rate ratio was 1·76 (0·62-4·03).”
Thus the rate of seroconversions in discordant relationships was very little higher than overall; evidently the rate of seroconversion in non-discordant relationships was appreciable. “HIV” was appearing in absence of “HIV”.

AGAIN: The obvious inference, consistent with large amounts of other data, is that pregnancy per se is a condition that conduces to testing “HIV-positive”. Pregnancy is one of many conditions that conduce to testing “HIV-positive” (see Why pregnant women tend to test “HIV-positive”, 5 October 2009).


Under mainstream HIV/AIDS theory, then,


An irreverent observer might express this as


or as Axel put it,

the virgin birth of “HIV”


P.S. re condoms:
Alert and wary consumers of data will have noted in the Table above not only that pregnant women become “HIV”-positive more often than others, but also that women who used condoms (regularly or irregularly) became “HIV”-positive more often than those who never used condoms.
Just another unacknowledged self-contradiction in HIV/AIDS theory.

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